We demonstrated high levels of sclerostin in thyrotoxicosis and a significant decrease of its serum concentrations coinciding with restoration of an euthyroid state. Pretreatment sclerosin levels in our study were higher than reference values presented by Biomedica (mean concentration - 19.3 pmol/l, range from 10.9 pmol/l to 28.7 pmol/l in serum), and by other authors - 33–37 pmol/l for healthy premenopausal women [6, 7] and 49.8 pmol/l - for men .
Thyrotoxicosis is a common endocrine disorder, affecting several systems and organs including skeletal system. Thyrotoxicosis increases bone metabolism and leads to development of osteoporosis [8–10]. Hyperthyroid patients have high bone turnover and negative calcium and phosphorus balance . These detrimental effects of thyrotoxicosis on bone metabolism are probably caused by overproduction of T3, mediated principally by T3 receptor alpha  or low TSH level [13, 14].
There are several examples of negative impact of thyrototoxicosis on bones even, in subclinical hyperthyroidism, for instance low-normal TSH values are associated with high prevalence of vertebral fractures in women with post-menopausal osteoporosis or osteopenia, independently of thyroid hormones, age and BMD value . This is one of the reasons why in subclinical hyperthyroidism treatment should be considered in the presence of risk factors, including osteoporosis .
Influence of thyrotoxicosis on bone seems to be temporary. Fracture risk was only significantly increased around the time of diagnosis but decreased to normal levels after restoration of an euthyroid state [9, 10]. Furthermore, normalization of BMD, bone markers and osteoprotegerin was observed during treatment [10, 11, 16], however, some authors showed elevation of bone formation markers despite normalization of thyroid hormones and TSH levels [10, 17]. We speculate that a decrease of sclerostin levels – as observed by us - may be associated with normalization of bone metabolism. It may also be argued that the above mentioned decrease in sclerostin levels in patients recovering from thyrotoxicosis might be mediated by PTH. This is because a fall of PTH concentration was reported in subjects with thyrotoxicosis [10, 17], followed by an increase during anti-thyroid treatment . There are also recent data demonstrating a decline of sclerostin concentrations by PTH. For instance, lowering of sclerostin levels was demonstrated after injection of PTH  and in patients with hyperparathyroidism [18, 19]. Supposing the normalization of thyroid hormones is accompanied by an increase of PTH, one might argue that PTH per se might be responsible for the decline of sclerostin concentrations observed, in our study.
To the best of our knowledge, this study is the first in which a clear decrease in sclerostin concentrations resulting presumably from a decrease of thyroid function has been demonstrated. The cause of this phenomenon is, however, complex and requires further study.